PATHOGENESIS OF THE GLOMERULONEPHRITIS OF NZB/W MICE
PATHOGENESIS OF THE GLOMERULONEPHRITIS OF NZB/W MICE
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NZB/W 小鼠肾小球肾炎的发病机制
DOI：
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发表时间：
1968
影响因子：
15.3
通讯作者：
Frank J. Dixon
中科院分区：
文献类型：
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作者：
P. H. Lambert;Frank J. Dixon
NZB/W小鼠肾小球肾炎的发生与抗核抗体，特别是抗DNA抗体的形成密切相关。发展中的炎性肾小球病变的特征是γG-和β 1C-球蛋白加上DNA和可能的其他核抗原，可能作为复合物，以颗粒状至荧光状的模式沿着毛细血管壁和系膜沉积。洗脱研究显示肾小球中的γ G-球蛋白主要是可溶性核抗原的γ G2 A型抗体。用DNA-甲基化BSA主动免疫年轻NZB/W小鼠，增强抗核抗体应答，加速肾小球肾炎的发展并增加其严重性。同样，将可溶性DNA注射到具有循环抗DNA抗体但肾炎尚未严重的NZB/W小鼠中，会导致肾炎迅速进展。
The development of glomerulonephritis in NZB/W mice is closely related to the formation of antinuclear, particularly anti-DNA, antibodies. The developing inflammatory glomerular lesions are characterized by the deposition of γG- and β1C-globulins plus DNA and possibly other nuclear antigens, presumably as complexes, in a granular to lumpy pattern along the capillary walls and in the mesangia. Elution studies revealed the γG-globulin in the glomeruli to be largely γG2A-type antibody to soluble nuclear antigens. Enhancement of the antinuclear antibody response by active immunization of young NZB/W mice with DNA-methylated BSA hastens the development and increases the severity of the glomerulonephritis. Similarly, injections of soluble DNA into NZB/W mice with circulating anti-DNA antibodies but with as yet little nephritis causes rapid progression of nephritis.